Programmed cell death 1 (PD-1) plays a crucial role in immune checkpoint inhibitor therapies, enhancing T-cell activity by blocking its signaling. PD-1 inhibitors are approved for various cancers, but their functions can differ among cell types. Merkel cell carcinoma (MCC), a rare skin cancer, responds well to PD-1 inhibitors, but it was unclear if MCC cells express PD-1 and how it affects tumor growth.
Researchers from Brigham and Women's Hospital conducted a study, discovering that PD-1 expression on MCC cells accelerates tumor growth by activating the mTOR pathway and generating reactive oxygen species. Inhibiting mTOR and neutralizing reactive oxygen species suppressed tumor proliferation in mice. These findings could lead to new treatments for MCC, benefitting patients without T-cell immunity.
Corresponding author Tobias Schatton stated, "Our work identifies PD-1 as an MCC-intrinsic receptor that promotes tumor growth, and targeting this tumor-intrinsic PD-1 signaling network could improve MCC patient outcomes."
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